Saint-Petersburg State Pediatric

Medical Academy
Department of Faculty
Surgery
Chronic pancreatitis and
pseudocysts.
Assistant of Professor
Dr. Ivanov Artem L.
 Chronic pancreatitis
Definition
 Chronic pancreatitis - chronic
inflammation causes fibrosis with
destruction of exocrine parenchyma leading
to malabsorption and steatorrhoea. In the
later stages, diabetes mellitus may follow
destruction of the endocrine parenchyma.
 The prospective Copenhagen Pancreatitis
Study found an annual incidence of 8.2
cases per 100000 and a prevalence of 27.4
per 100000.
Acute and chronic pancreatitis are
distinguished from each other on the basis of
structural and functional criteria. In acute
pancreatitis, the gland is normal before the
attack and can return to normal after
resolution of the attack, whereas in chronic
pancreatitis, the gland is abnormal before or
after the attack, or both.
This classification scheme does not depend on
how rapidly symptoms appear or resolve, or on
the severity of the symptoms. Thus, it may be
impossible to distinguish an exacerbation of
chronic pancreatitis from an attack of acute
pancreatitis on clinical grounds alone.
 A B

Panel A shows normal pancreatic tissue, and Panel B shows changes of chronic
pancreatitis, characterized by a marked increase in interlobular fibrous tissue, atrophy
of the acini, and chronic inflammatory infiltrate. (Hematoxylin and eosin, x95.)

The morphologic changes of chronic pancreatitis (Figure 1A and Figure 1B)

include varying degrees of edema, acute inflammation, and necrosis,
superimposed on a background of chronic changes that include fibrosis,
inflammation, and loss of exocrine tissue. Ductal elements may be dilated, and
intraductal protein plugs, which may be calcified, can be seen. Most
investigators believe that acute pancreatitis does not lead to chronic pancreatitis
unless complications, such as pseudocysts or ductal strictures, are present.
 Aetiology
 Alcohol accounts for up to 80% of all cases of
chronic pancreatitis.
In developed countries, 60 to 70 percent of patients
with chronic pancreatitis have a long history (6 to
12 years) of heavy consumption of alcohol (150 to
175 g per day) before the onset of clinically
apparent disease. A high-protein diet with either a
very high or very low fat content may potentiate
the injurious effects of alcohol. Like alcoholism
itself, alcohol-induced pancreatitis is most
frequent among men, and it has its peak incidence
between 35 and 45 years of age.
 Aetiology
Other causes include:
 congenital - pancreas divisum; annular pancreas
 hereditary - sometimes with cyclical neutropenia
 cystic fibrosis - in young adults
 hypercalcaemia
 hyperlipidaemia
 obstruction of the pancreatic duct can cause chronic
pancreatitis.
 mechanical or structural changes of the pancreatic - duct
sphincter, pseudocysts, post - traumatic ductal strictures,
periampullary tumours.
 gallstones is an uncommon cause.
 a pancreas divisum is a very rare cause.
 idiopathic - 30 - 40% of patients; tend to cluster in two
groups - a younger group (with peak incidence of 15 - 30
years of age) and an older group (peak of 50 - 70 years).
 Pathogenesis
 The hypersecretion of protein from acinar cells in the absence of
increased fluid or bicarbonate secretion from duct cells is
characteristic of chronic pancreatitis.
 Lithostathine (formerly called pancreatic-stone protein) is a
14,000-dalton protein that is secreted by acinar cells and is
present in large amounts in pancreatic-juice precipitates, ductal
plugs, and stones.
 Patients with idiopathic chronic pancreatitis frequently have
elevated pressure in the pancreatic duct, suggesting that ductal
"hypertension" may play an important part in chronic
pancreatitis. The results of manometry of the sphincter of Oddi
are usually normal under these conditions, suggesting that
dysfunction of the sphincter is not the explanation for the elevated
pressure. It is possible that papillary stenosis or ductal
obstruction by plugs or stones could result in ductal hypertension,
but the mechanisms by which these changes could lead to
inflammation and fibrosis are not known.
 Symptoms
 Abdominal pain
 Greatest in the upper abdomen
 May last from hours to days
 Eventually may be continuous
 May be worsened by eating or drinking
 May be worsened by alcohol consumption
 May radiate to the back
 Nausea and vomiting
 Unintentional weight loss
 Fatty stools
Sitting up and leaning forward may sometimes relieve the
abdominal pain associated with pancreatitis.
Pale or clay-colored stools may also be associated with
this condition.
 Exams and Tests
 Serum lipase may be higher than normal, but can
return to normal as the disease gets worse.
 Serum amylase may be higher than normal, but
can return to normal as the disease gets worse.
 Serum trypsinogen may be low.
 Fecal fat test shows fatty stools.
Inflammation or calcium deposits of the pancreas
may be evident on:
 Abdominal CT scan
 Abdominal ultrasound
 ERCP
 An exploratory laparotomy may be done to
confirm the diagnosis of pancreatitis.
Lab Studies:

Blood tests
Serum amylase and lipase levels may be slightly elevated in
chronic pancreatitis; high levels are found only during acute
attacks of pancreatitis. In the later stages of chronic
pancreatitis, atrophy of the pancreatic parenchyma can result
in normal serum enzyme levels, because of significant fibrosis
of the pancreas, resulting in decreased concentrations of these
enzymes within the pancreas.
While low concentrations of serum trypsin are relatively
specific for advanced chronic pancreatitis, they are not
sensitive enough to be helpful in most patients with mild-to-
moderate disease.
Laboratory studies to identify causative factors include serum
calcium and triglyceride levels.
When common etiologies are not found, research protocols
are available to test for genetic mutations in cationic
 Plain Radiograph of the Abdomen Showing Diffuse
Calcifications throughout the Pancreas (Arrows) in an
Alcoholic Patient with Chronic Pancreatitis.
CT scan of the upper abdomen showing
multiple white-colored calcifications.
These occur in chronic pancreatitis.
 Endoscopic retrograde cholangiopancreatography (ERCP) is an endoscopic
procedure used to identify the presence of stones, tumors, or narrowing in the
biliary and pancreatic ducts. After the endoscope is properly placed, a
catheter is advanced which will inject a contrast agent through the ducts. The
contrast is visible on X-rays, and allows a physician to evaluate the caliber,
length and course of the ducts. An ERCP may be performed if a patient
experiences symptoms such as jaundice, abdominal pain, fever, or
During an endoscopic retrograde cholangiopancreatography,
a catheter is advanced through the endoscope and inserted
into the pancreatic or biliary ducts. A contrast agent is
injected into these ducts and X-rays are taken to evaluate
their caliber, length and course. Narrowing, stones, and
tumors in the ducts can be identified in the X-rays.
 ERCP

 An abnormal endoscopic retrograde cholangiopancreatography (ERCP), a

type of x-ray of the biliary tract, shows irregular flow of white dye,
indicating strictures in the pancreatic duct. This finding is typical of
pancreatitis.
Endoscopic Retrograde Pancreatograms.
Panel A shows a normal subtraction endoscopic retrograde pancreatogram that
reveals the filling of normal side branches and a smooth, nondilated main ductal
system. Panel B shows an endoscopic retrograde pancreatogram in a patient
with chronic pancreatitis, revealing a dilated, tortuous main duct that contains
stones or protein plugs (lucencies in duct marked by short thin arrows). A
stricture is visible in the midportion of the duct (long thin arrow). Note the
dilatation of the uncinate-process branch (thick arrow).
 Treatment
 The different treatment modalities for management
of chronic pancreatitis are medical measures,
therapeutic endoscopy and surgery. Treatment is
directed, when possible, to the underlying cause, and
to relief of the pain and malabsorption.
 Pancreatic Enzyme Supplementation

Replacement pancreatic enzymes are often effective in

treating the malabsorption and steatorrhea.
However, the outcome from 6 randomized trials has
been inconclusive with uncertain benefits to the
patients. Treatment is directed, when possible, to the
underlying cause, and to relief of the pain and
malabsorption.
Endoscopy
Therpeutic ERCP is viewed as an attractive
alternative to surgery because it is less
invasive and requires a shorter hospitalization
period.
Endoscopic therapy might be beneficial in
chronic pancreatitis with the following:
Papillary stenosis: In a subset of patients with
chronic pancreatitis, the papillary sphincter
pressure and pancreatic ductal pressure are
increased. In appropriately selected patients, a
pancreatic duct sphincterotomy will facilitate
drainage, reduce ductal pressures, and may
help alleviate pain.
 Pancreatic duct strictures: Suitable candidates for endoscopic
therapy are patients with a dominant distal pancreatic
stricture and upstream ductal dilatation. The procedure
involves placing a guidewire through the stricture into the
proximal duct, performing a pancreatic sphincterotomy,
dilating the stricture, and placing a stent. While technical
success is achieved in more than 90% of patients, nearly 20%
will have a complication and less than two thirds of patients
benefit clinically; pain relief correlates with a reduction in the
diameter of the duct by more than 2 mm. Patients with
recurrent pancreatitis are more likely to benefit than those
with chronic daily pain. The stricture rarely disappears, and
the stent invariably clogs; therefore, repeated procedures are
required to exchange it. Prolonged or inappropriate stenting
can injure the pancreatic duct.
 Pancreatic duct stones: While pancreatic duct
stones are sequelae of chronic pancreatitis, they
also may be responsible for recurrent acute
pancreatitis or exacerbations of chronic pain
related to ductal obstruction and increased ductal
pressure. Stones usually form proximal to ductal
strictures and usually require a pancreatic duct
sphincterotomy and stricture dilation to enable
their extraction. In addition to various endoscopic
techniques, extracorporeal shockwave lithotripsy
often is necessary to break up impacted or large
stones into smaller pieces suitable for removal.
Technical success is achieved in approximately
60% of patients, complications occur in 20%, and
approximately 70% of patients report
improvement in their symptoms.
 Surgical treatment of chronic pancreatitis: The choice
of operation depends on the clinical problem and
preoperative assessment of the abnormality. In
general, the approach aims either to improve
pancreatic duct drainage or to resect the diseased
organ.
 Pancreatic duct drainage: In patients with a dilated
pancreatic duct, a Roux-en-Y side-to-side
pancreaticojejunostomy is indicated. The operative
mortality rate is about 3%, and pain relief is obtained in
approximately 75% of patients (patients' cases were
followed for a mean of 8 y). Pancreatic dysfunction
progresses similarly in surgical and nonsurgical groups,
suggesting that drainage procedures do not affect the
natural evolution of the disease significantly. The long-term
result for pain relief is reported as 42% of patients.
 Pancreatic resection: If the disease is limited to
the head of the pancreas, a Whipple operation
(pancreaticoduodenectomy) can produce good
results. In patients with intractable pain and
diffuse disease with nondilated ducts, a subtotal
or total pancreatectomy can be offered; however,
pancreatic function and quality of life are
impaired after these procedures, and the
operative mortality rate of total pancreatectomy
is about 10%. Pain is treated successfully in
approximately 70% of cases.
 Total pancreatectomy and islet autotransplantation: In
selected patients, the long-term morbidity caused by
diabetes following total pancreatectomy can be avoided.
This involves harvesting the islets from the resected
pancreas and injecting them into the portal system,
which then lodges them in the liver. In 46 patients
undergoing near-total pancreatectomy, pain relief
occurred in 82% (resolved in 39% and improved in
43%). Although 51% were insulin independent initially,
this decreased to 34% (one third) from 2-10 years after
transplantation. Increasing severity of pancreatic
fibrosis correlates positively with poor recovery of islets
(<300,000) and insulin dependence.
 Pancreatic pseudocyst
 A pancreatic pseudocyst is a circumscribed
collection of fluid rich in amylase and other
pancreatic enzymes, blood and necrotic tissue
typically located in the lesser sac. It has a non-
epithelialised lining made of granulation tissue and
hence the name pseudocyst (pseudo - false).
 By contrast, true cysts have an epithelial lining.
 This is typically a complication of acute pancreatitis,
but may also occur following abdominal trauma.
Pancreatic pseudocysts account for approximately
75% of all pancreatic masses.
 Etiopathogenesis

 Acute pancreatitis results amongst other things in the

disruption of pancreatic parenchyma and the ductal system.
This results in extravasation of pancreatic enzymes which in
turn digest the adjoining tissues. This results in a collection of
fluid containing pancreatic enzymes, hemolysed blood and
necrotic debris around the pancreas. The lesser sac being a
potential space, the fluid collects here preferentially. This is
called an acute pancreatic collection. Some of these collections
resolve on their own as the patient recovers from the acute
episode. However, others become more organised and get
walled-off within a thick wall of granulation tissue and fibrosis.
This takes several weeks to occur and results in a pancreatic
pseudocyst.
 Pseudocyst

 A pseudocyst of the pancreas is seen as the

dark oval (arrows) structure in the area of the
head of the pancreas.
 Dynamic Computed Tomographic Image Showing a Thin-
Walled Pancreatic Pseudocyst (Thick Arrow) Compressing the
Gastric Antrum and an Abnormal Pancreas with Ductal
Dilatation and Calcifications (Thin Arrows).
 Treatment
A small pseudocyst that is not causing any
symptoms may be managed conservatively.
However, a large proportion of them will need
some form of treatment, The interventions
available are:
 Endoscopic trans-gastric drainage

 Imaging guided percutaneous drainage

 Laparoscopic/open cystogastrostomy